Associations between food portion sizes, insulin resistance, VO2 max and metabolic syndrome in European adolescents: The HELENA study.

BACKGROUND AND AIMS: This study aims to examine the associations of food portion size (PS) with markers of insulin resistance (IR) and clustered of metabolic risk score in European adolescents. METHODS: A total of 495 adolescents (53.5% females) from the Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) study were included. The association between PS from food groups and homeostasis model assessment of insulin resistance (HOMA-IR) index, VO2 max, and metabolic risk score was assessed by multilinear regression analysis adjusting for several confounders. Analysis of covariance (ANCOVA) was used to determine the mean differences of food PS from food groups by HOMA-IR cutoff categories by using maternal education as a covariable. RESULTS: Larger PS from vegetables in both gender and milk, yoghurt, and milk beverages in males were associated with higher VO2 max, while larger PS from margarines and vegetable oils were associated with lower VO2 max (p < 0.05). Males who consumed larger PS from fish and fish products; meat substitutes, nuts, and pulses; cakes, pies, and biscuits; and sugar, honey, jams, and chocolate have a higher metabolic risk score (p < 0.05). Males with lower HOMA-IR cutoff values consumed larger PS from vegetables, milk, yoghurt, and milk beverages (p < 0.05). Females with lower HOMA-IR cutoff values consumed larger PS from breakfast cereals, while those with higher HOMA-IR cutoff values consumed larger PS from butter and animal fats (p = 0.018). CONCLUSION: The results show that larger PS from dairy products, cereals, and high energy dense foods are a significant determinant of IR and VO2 max, and larger PS from food with higher content of sugar were associated with higher metabolic risk score.

[Maternal nutrition during pregnancy conditions the fetal pancreas development, hormonal status and diabetes mellitus and metabolic syndrome biomarkers at birth]. / La alimentación de la madre durante el embarazo condiciona el desarrollo pancreático, el estatus hormonal del feto y la concentración de biomarcadores al nacimiento de diabetes mellitus y síndrome metabólico.

Pregnancy is a vital period where several hyperplasic, hypertrophic processes together with metabolic adaptation and preparation for extra-uterine life take place. Present review accounts for central aspects of nutrition throughout gestation on the embryonic and fetal periods. It is centered in the major changes occurring in fetal pancreas, with special mention to the susceptibility of this main glucose homeostasis organ to support nutritional changes during maturation and development. Studies performed in animal models as human are commented considering the role of maternal nutrition on ß-cell mass size, insulin and other pancreatic hormones production, and insulin sensitivity. Details of both the thrifty genotype and phenotype hypothesis are given, indicating that hypo/subnutrition causes metabolic adaptations that permit the future body to grow and develop itself in limited environmental and energetic conditions. The Barker hypothesis is considered suggesting that this metabolic hypothesis is a double-edged sword in the actual abundance World. Lastly the review, taking into account our own research and other papers, analyses less known aspects that relate maternal diet with insulin resistance/sensitivity markers at delivery. Particularly the role of the saturated fatty acid/carbohydrate and omega-6/omega-3 ratios in the frame of maternal diet is reviewed considering the quality of those diets under the Healthy Eating Index and the Adherence to Mediterranean Diet scores and the relationship with insulin resistance profile at birth. Present review ends indicating that nutritional habits should be strongly stated before gestation in order to assure a proper nutrition since the first moment of pregnancy. This will support an adequate fetal and pancreatic growth and development, and in turn, adequate glucose homeostasis during pregnancy and later in life, slowing down or preventing from degenerative diseases related with metabolic syndrome and type 2 diabetes mellitus.

El embarazo es una etapa de vital importancia, donde tienen lugar múltiples procesos hiperplásicos, hipertróficos, de adaptación metabólica y de preparación para la vida extrauterina. En esta revisión se analizan aspectos centrales de la nutrición durante el embarazo, tanto en la etapa embrionaria como fetal. Se exponen los cambios más importantes que tienen lugar en el páncreas fetal, con especial mención de la susceptibilidad de este órgano central en la homeostasis de la glucosa a enfrentarse a cambios nutricionales durante su desarrollo y maduración. Se comentan algunos estudios realizados en modelos animales y en la especie humana con especial mención del papel de la nutrición materna sobre la masa de células-ß, la producción de insulina y otras hormonas y la sensibilidad a la insulina. Se detallan aspectos sobre las hipótesis del genotipo y fenotipo ahorrador, señalando que la hiponutrición causa adaptaciones metabólicas que permiten al futuro ser medrar en un ambiente de nutrientes y energía reducido. Se revisan algunos aspectos de la hipótesis de Barker y se indica que la adaptación metabólica que preconiza es un arma de doble filo en el mundo actual de abundancia que nos encontramos. Por último se revisan trabajos de nuestro grupo y de otros autores, en aspectos menos estudiados que relacionan la calidad de la dieta materna con alteraciones de marcadores de resistencia/sensibilidad a la insulina en el momento del parto. En especial se estudia el papel de la relación ácidos grasos saturados/hidratos de carbono y la de ácidos grasos omega-6/omega-3 en el marco de dietas inadecuadas bajo el punto de vista del índice de alimentación saludable o de la adherencia a la dieta mediterránea que condicionan en el neonato un perfil de resistencia a la insulina. La revisión incide además en que los hábitos nutricionales deben estar fuertemente instaurados ya en la etapa pregestacional para asegurar una buena alimentación desde las primeras semanas del embarazo, y asegurar un desarrollo fetal y en particular pancreático que posibilite una homeostasis adecuada de la glucosa durante el embarazo y en etapas posteriores de la vida evitando, o al menos frenando, el desarrollo y la instauración de enfermedades degenerativas asociadas con el síndrome metabólico y la diabetes tipo 2.

La alimentación de la madre durante el embarazo condiciona el desarrollo pancreático, el estatus hormonal del feto y la concentración de biomarcadores al nacimiento de diabetes mellitus y síndrome metabólico / Maternal nutrition during pregnancy conditions the fetal pancreas development, hormonal status and diabetes mellitus and metabolic syndrome biomarkers at birth

El embarazo es una etapa de vital importancia, donde tienen lugar múltiples procesos hiperplásicos, hipertróficos, de adaptación metabólica y de preparación para la vida extrauterina. En esta revisión se analizan aspectos centrales de la nutrición durante el embarazo, tanto en la etapa embrionaria como fetal. Se exponen los cambios más importantes que tienen lugar en el páncreas fetal, con especial mención de la susceptibilidad de este órgano central en la homeostasis de la glucosa a enfrentarse a cambios nutricionales durante su desarrollo y maduración. Se comentan algunos estudios realizados en modelos animales y en la especie humana con especial mención del papel de la nutrición materna sobre la masa de células-β, la producción de insulina y otras hormonas y la sensibilidad a la insulina. Se detallan aspectos sobre las hipótesis del genotipo y fenotipo ahorrador, señalando que la hiponutrición causa adaptaciones metabólicas que permiten al futuro ser medrar en un ambiente de nutrientes y energía reducido. Se revisan algunos aspectos de la hipótesis de Barker y se indica que la adaptación metabólica que preconiza es un arma de doble filo en el mundo actual de abundancia que nos encontramos. Por último se revisan trabajos de nuestro grupo y de otros autores, en aspectos menos estudiados que relacionan la calidad de la dieta materna con alteraciones de marcadores de resistencia/sensibilidad a la insulina en el momento del parto. En especial se estudia el papel de la relación ácidos grasos saturados/hidratos de carbono y la de ácidos grasos omega-6/omega-3 en el marco de dietas inadecuadas bajo el punto de vista del índice de alimentación saludable o de la adherencia a la dieta mediterránea que condicionan en el neonato un perfil de resistencia a la insulina. La revisión incide además en que los hábitos nutricionales deben estar fuertemente instaurados ya en la etapa pregestacional para asegurar una buena alimentación desde las primeras semanas del embarazo, y asegurar un desarrollo fetal y en particular pancreático que posibilite una homeostasis adecuada de la glucosa durante el embarazo y en etapas posteriores de la vida evitando, o al menos frenando, el desarrollo y la instauración de enfermedades degenerativas asociadas con el síndrome metabólico y la diabetes tipo 2 (AU)

Pregnancy is a vital period where several hyperplasic, hypertrophic processes together with metabolic adaptation and preparation for extra-uterine life take place. Present review accounts for central aspects of nutrition throughout gestation on the embryonic and fetal periods. It is centered in the major changes occurring in fetal pancreas, with special mention to the susceptibility of this main glucose homeostasis organ to support nutritional changes during maturation and development. Studies performed in animal models as human are commented considering the role of maternal nutrition on β-cell mass size, insulin and other pancreatic hormones production, and insulin sensitivity. Details of both the thrifty genotype and phenotype hypothesis are given, indicating that hypo/subnutrition causes metabolic adaptations that permit the future body to grow and develop itself in limited environmental and energetic conditions. The Barker hypothesis is considered suggesting that this metabolic hypothesis is a double-edged sword in the actual abundance World. Lastly the review, taking into account our own research and other papers, analyses less known aspects that relate maternal diet with insulin resistance/sensitivity markers at delivery. Particularly the role of the saturated fatty acid/carbohydrate and omega-6/omega-3 ratios in the frame of maternal diet is reviewed considering the quality of those diets under the Healthy Eating Index and the Adherence to Mediterranean Diet scores and the relationship with insulin resistance profile at birth. Present review ends indicating that nutritional habits should be strongly stated before gestation in order to assure a proper nutrition since the first moment of pregnancy. This will support an adequate fetal and pancreatic growth and development, and in turn, adequate glucose homeostasis during pregnancy and later in life, slowing down or preventing from degenerative diseases related with metabolic syndrome and type 2 diabetes mellitus (AU)

Maternal diets with low healthy eating index or Mediterranean diet adherence scores are associated with high cord-blood insulin levels and insulin resistance markers at birth.

BACKGROUND/OBJECTIVES: Few studies have used healthy eating index (HEI) and mediterranean diet adherence (MDA) scores to evaluate the diet quality during pregnancy. To determine the relationship between first trimester diet quality and insulin sensitivity/resistance biomarkers at birth. SUBJECTS/METHODS: Cord-blood insulin sensitivity/resistance biomarkers of the offspring of 35 women whose diets were 'adequate' or 'inadequate' according to their HEI score (>70 or ≤ 70, respectively) and their 13-point MDA score (≥ 7 or <7, respectively). RESULTS: Low HEI-score diets contained less (g/1000 kcal) carbohydrates (CHO; P=0.027) and fibre (P=0.011), and more fats (P<0.001) and cholesterol (P<0.001), and contributed (percentage contribution to total energy (%En)) fewer CHO (P=0.005), more fats (P=<0.001) and saturated fatty acid (SFA; P=0.002) than their high HEI-score counterparts. Low MDA-score diets contained less (g/1000 kcal) fibre (P<0.001) and more cholesterol (P=0.05), had lower polyunsaturated fatty acids+monounsaturated fatty acid/SFA (PUFA+MUFA/SFA; P=0.05) and higher SFA/CHO (P=0.021) and ω-6/ω-3 PUFA ratios (P=0.044) than their respective counterparts. Women consuming the low HEI- or low MDA-score diets had low-fasting glycaemia (P=0.016 or P=0.025, respectively) but delivered infants with high insulinaemia (P=0.048 or P=0.017, respectively), homeostatic model assessment for insulin resistance (HOMA-IR; P=0.031 or P=0.049, respectively) and glycaemia (P=0.018 or P=0.048, respectively). The relative risk (RR) of high-neonatal glycaemia and insulinaemia were 7.6 (P=0.008) and 6.7 (P=0.017) for low vs high HEI-score groups. High HOMA-IR and high glucose RR were, respectively, 3.4 (P=0.043) and 3.9 (P=0.016) in neonates from the <7 MDA- vs ≥ 7 MDA-score group. These RRs were not affected by potential confounders. CONCLUSION: Maternal diets with low HEI- or MDA-scores during the first trimester of pregnancy negatively affect insulin resistance markers at birth.

Effects of maternal glucose tolerance, pregnancy diet quality and neonatal insulinemia upon insulin resistance/sensitivity biomarkers in normoweight neonates / Efectos de la tolerancia a la glucosa y calidad de la dieta materna durante embarazo y de los niveles de insulina al nacimiento sobre biomarcadores de resistencia/sensibilidad a la insulina en neonatos normopeso

Introduction: Differences in neonatal insulin sensitivity/resistance markers due to the maternal impaired glucose tolerance (IGT) have not been tested. The Healthy Eating Index (HEI) score has been employed for evaluating pregnancy diet quality. Aims: To study, the effect of neonatal insulinemia, maternal IGT and diet HEI score upon insulin sensitivity/resistance at birth. Methods: 176 singleton, normoweight, full-term, Caucasian Spanish neonates, delivered without fetal distress whose mothers were screened for gestational IGT were studied. Quantitative Insulin Sensitivity Check Index (QUICKI) and Homeostatic Model Assessment (HOMAIR) were calculated. Diet followed during the third month of pregnancy was recorded and the respective HEI score calculated in a sample of 29 mothers. Results: As quartile for cord blood insulin levels increased, glucose, the insulin/cortisol ratio and HOMA-IR(all p < 0.001) and IGF-I (p < 0.01) increased while QUICKI and the glucose/insulin ratio (both p < 0.001) and GH (p <0.05) decreased. Neonates from IGT mothers had higher insulin, HOMA-IR (both p < 0.01) and insulin/cortisol ratio(p < 0.05) and lower GH, QUICKI (both p < 0.01) and glucose/insulin ratio (p < 0.05) than their normal maternal glucose tolerance (NGT) counterparts. Neonatal insulinemia influences more than IGT on the insulin resistance/sensitivity markers at birth. Mothers of hyperinsulinemic neonates showed lower HEI scores (p < 0.05).Conclusion: A large percentage of full-term normoweightinfants with hyperinsulinemia showed altered insulin resistance markers. Their mothers consumed low quality diets. Screening strategies focused on neonatal glycemia and insulinemia together with maternal nutritional assessment and advice during pregnancy should be considered (AU)

Introducción: Los efectos de la disminución de la tolerancia a la glucosa (DTG) materna sobre la insulinorresistencia neonatal han sido poco estudiados. La puntuación del Índice de Alimentación Saludable (HEI) es útil para evaluar la calidad de la dieta en gestantes. Objetivos: Estudiar la asociación de insulinemia neonatal y DTG materna con la resistencia/sensibilidad a la insulina al nacimiento y con el HEI materno. Métodos: Se estudiaron 176 neonatos españoles, caucásicos, a término, normopeso, de embarazo único y sin distrés fetal, cuyas madres fueron cribadas para DTG en elembarazo. Se calcularon el Quantitative Insulin Sensitivity Check Index (QUICKI) y el Homeostatic Model Assessment (HOMA-IR). En 29 madres se estudió la dieta consumida durante el tercer mes de gestación y se calculó su respectivo HEI. Resultados: Al aumentar el cuartil de insulina en sangre de cordón, aumentaron glucosa, cociente insulina/cortisol, HOMA-IR (p < 0,001) e IGF-I (p < 0,01), y disminuyeron QUICKI y cociente glucosa/insulina (p < 0,001) y GH (p < 0,05). Los neonatos de madres con DTG tuvieron mayores niveles de insulina, HOMA-IR (p < 0,01) y cociente insulina/cortisol (p < 0,05) y menores de GH,QUICKI (p < 0,01) y el cociente glucosa/insulina (p < 0,05)que los de madres con tolerancia a la glucosa normal. La insulinemia neonatal influye más en los marcadores de resistencia/sensibilidad a la insulina que la DTG. Las madres de los niños hiperinsulinémicos tuvieron HEI más bajos (p < 0,05). Conclusiones: Un gran porcentaje de neonatos con hiperinsulinemia muestran marcadores de insulinorresistencia alterados. Sus madres ingirieron dietas de baja calidad. Debe considerarse la necesidad del cribado de glucosa e insulina en estos neonatos y el asesoramiento y evaluación nutricional durante el embarazo (AU)

Effects of maternal glucose tolerance, pregnancy diet quality and neonatal insulinemia upon insulin resistance/sensitivity biomarkers in normoweight neonates.

INTRODUCTION: Differences in neonatal insulin sensitivity/ resistance markers due to the maternal impaired glucose tolerance (IGT) have not been tested. The Healthy Eating Index (HEI) score has been employed for evaluating pregnancy diet quality. AIMS: To study, the effect of neonatal insulinemia, maternal IGT and diet HEI score upon insulin sensitivity/ resistance at birth. METHODS: 176 singleton, normoweight, full-term, Caucasian Spanish neonates, delivered without fetal distress whose mothers were screened for gestational IGT were studied. Quantitative Insulin Sensitivity Check Index (QUICKI) and Homeostatic Model Assessment (HOMAIR) were calculated. Diet followed during the third month of pregnancy was recorded and the respective HEI score calculated in a sample of 29 mothers. RESULTS: As quartile for cord blood insulin levels increased, glucose, the insulin/cortisol ratio and HOMA-IR (all p < 0.001) and IGF-I (p < 0.01) increased while QUICKI and the glucose/insulin ratio (both p < 0.001) and GH (p < 0.05) decreased. Neonates from IGT mothers had higher insulin, HOMA-IR (both p < 0.01) and insulin/cortisol ratio (p < 0.05) and lower GH, QUICKI (both p < 0.01) and glucose/ insulin ratio (p < 0.05) than their normal maternal glucose tolerance (NGT) counterparts. Neonatal insulinemia influences more than IGT on the insulin resistance/sensitivity markers at birth. Mothers of hyperinsulinemic neonates showed lower HEI scores (p < 0.05). CONCLUSION: A large percentage of full-term normoweight infants with hyperinsulinemia showed altered insulin resistance markers. Their mothers consumed low quality diets. Screening strategies focused on neonatal glycemia and insulinemia together with maternal nutritional assessment and advice during pregnancy should be considered.